Related Experiment Video
Updated: Jun 18, 2026
06:31
Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
Published on: June 2, 2023
MicroRNA-7 modulates CD98 expression during intestinal epithelial cell differentiation
Hang Thi Thu Nguyen1, Guillaume Dalmasso, Yutao Yan
1Department of Medicine, Division of Digestive Diseases, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
The Journal of Biological Chemistry
|November 7, 2009
Summary
MicroRNAs, specifically microRNA-7, regulate CD98 expression in intestinal cells. This finding is crucial for understanding cell adhesion and offers potential therapeutic targets for inflammatory bowel diseases.
Area of Science:
- Cell Biology
- Molecular Biology
- Gastroenterology
Background:
- Transmembrane glycoprotein CD98 is vital for cellular functions like signaling and adhesion.
- MicroRNAs post-transcriptionally regulate gene expression, impacting cell differentiation, proliferation, and apoptosis.
Purpose of the Study:
- To investigate the role of microRNAs in regulating CD98 expression during intestinal epithelial cell differentiation and inflammation.
- To elucidate the mechanism by which microRNAs control CD98 expression in the intestine.
Main Methods:
- Utilized Caco2-BBE cell line for in vitro studies.
- Analyzed microRNA and CD98 expression in differentiated and undifferentiated cells.
- Investigated the effect of microRNA-7 on cell adhesion and CD98 overexpression.
- Examined microRNA and CD98 levels in mouse jejunum crypt and villus cells.
- Assessed expression changes in response to interleukin 1-beta stimulation.
- Compared microRNA-7 and CD98 levels in normal and Crohn disease colonic tissues.
Main Results:
- MicroRNA-7 directly targets and represses CD98 mRNA in Caco2-BBE cells.
- CD98 expression decreased while microRNA-7 increased during Caco2-BBE cell differentiation.
- Undifferentiated mouse crypt cells had higher CD98 and lower microRNA-706 than differentiated villus cells.
- MicroRNA-7 inhibited cell adhesion to laminin-1, an effect reversed by CD98 overexpression.
- Interleukin 1-beta reduced microRNA-7 levels, increasing CD98 expression.
- Inflamed Crohn disease tissues showed decreased microRNA-7 and increased CD98 levels.
Conclusions:
- MicroRNA-7 is a key regulator of CD98 expression during intestinal epithelial cell differentiation and inflammation.
- The microRNA-7/CD98 axis influences epithelial cell adhesion and migration.
- Dysregulation of this axis is implicated in intestinal inflammatory disorders like Crohn disease.
- MicroRNAs represent a promising therapeutic target for modulating CD98 in intestinal inflammation.
Related Concept Videos
01:22MicroRNAs
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
01:22MicroRNAs
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
01:22MicroRNAs
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
01:12Role Of Notch Signalling In Intestinal Stem Cell Renewal
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
01:23Renewal of Intestinal Stem Cells
The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
01:21Microbiota Modulation by Antibiotics
Antibiotics have revolutionized modern medicine by saving countless lives from bacterial infections. However, their widespread use has inadvertently harmed the delicate balance of the human gut microbiota. The gut microbiota, a complex community of bacteria, archaea, viruses, and fungi, plays a vital role in regulating metabolism, immune responses, and maintaining intestinal health. Antibiotics, especially broad-spectrum types, disrupt this ecosystem by eradicating both harmful and beneficial...